Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Flt-4 CRISPR/Cas9 KO Plasmid (h): sc-400684
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Flt-4 CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the Flt-4 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Flt-4 Antibody (E-3): sc-514825
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Flt-4 CRISPR/Cas9 KO Plasmid (h) | sc-400684 | 20 µg | $397.00 |
Overview
FLT4 encodes the receptor tyrosine kinase Flt-4 (VEGFR-3), a principal mediator of lymphangiogenic signaling downstream of VEGFC and VEGFD. Ligand-dependent activation triggers autophosphorylation and engages PI3K–AKT, MAPK/ERK, PLCγ, and related pathways that regulate endothelial cell survival, migration, and lymphatic vessel patterning. Flt-4 activity contributes to vascular and lymphatic development and is frequently examined in the context of tumor-associated lymphangiogenesis, metastatic dissemination, and inflammatory remodeling. Dysregulated FLT4 signaling has also been linked to inherited lymphatic disorders, supporting its use as a mechanistic node in vascular biology and disease models.
Flt-4 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FLT4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FLT4 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the FLT4 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish Flt-4 protein expression.
This CRISPR knockout system enables efficient generation of FLT4-deficient cell models for investigation of Flt-4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting FLT4 exon(s) critical for Flt-4 function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple FLT4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Flt-4 CRISPR/Cas9 KO Plasmid (h) and Flt-4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FLT4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Flt-4 HDR Plasmid (h) and Flt-4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FLT4 homology arms to support homology-directed repair at defined FLT4 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.